セッション情報 The 4th International Forum

I Drug-associated GI Injury:Advances of the pathogenesis and recent clinical topics 2. Recent clinical topics(b)Bowel injuries

タイトル IFI-2b-4:

Strategy of NSAID-induced small bowel lesions

演者 Higuchi Kazuhide(Second Department of Internal Medicine, Osaka Medical College, Japan)
共同演者 Takeuchi Toshihisa(Second Department of Internal Medicine, Osaka Medical College, Japan), Umegaki Eiji(Second Department of Internal Medicine, Osaka Medical College, Japan)
抄録 Non-steroidal anti-inflammatory drugs(NSAIDs)are known to cause mucosal damage not only in the stomach but also in the small intestine. Many questions remain to be answered about the pathogenesis and how to treat and prevent such mucosal damage to the small intestine. Animal studies have been used to elucidate the mechanisms underlying the mucosal damage induced by NSAIDs and suggest effective measures for its prevention. We evaluated the effects of a wide range of drugs used to treat peptic ulcers(including PG analogs, mucoprotective agents, histamine-2 receptor antagonists, proton-pump inhibitors [PPIs])on indomethacin-induced small-intestinal mucosal damage in rats. We found that mucoprotective agents such as rebamipide, teprenone, and irsogladine, as well as the PG analog misoprostol, significantly reduced small-intestinal damage in a dose-dependent manner. In addition, clinical studies have demonstrated significant efficacy for rebamipide, misoprostol, and irsogladine.
On the contrary, PPIs are standard treatment for NSAID-induced mucosal damage in the upper gastrointestinal tract. However, recent studies in rats have suggested that PPIs may not prevent NSAID-induced mucosal damage in the small intestine, and may even exacerbate it. There are no reports about the effects of long-term administration of PPIs during NSAID treatment on the human small intestine. We examined the time-course changes in capsule endoscopic findings of the small intestine during longer term treatment with a NSAID plus a PPI. During long-term NSAID treatment, co-administration of a PPI did not prevent the development of small-intestinal lesions. Repeated observations over a long-term period suggested that mucosal adaptation may occur in the small intestine.
Finally, we recommend as a strategy for NSAID-induced GI mucosal lesions,
1)for high risk patients with upper GI disease(peptic ulcer, reflux esophagitis)→PPI+mucoprotective drug
2)for not high risk patients→mucoprotective drug monotherapy
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